#10

What hormone levels and do you have links to these studies?
Common sense tells me this is false, that is not listed as a side effect. :thinking:

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#11

What did your doctor think of your LDL in January 2021? It was outside the reference range. I think it was above the 99th percentile. It was/is extremely high. 4.6 mmol/L is probably still around 94th percentile.

#12

The reference values differ between USA and Sweden. If I remember it correctly USA is much harder when it comes to keep for example LDL low. I don’t remember the argument why Sweden differ in this view but they have a reason for this.

This is what was said about my values:

"Your blood lipids generally look good. Your LDL cholesterol is slightly elevated, but your Apolipoprotein B value shows that the particles of LDL cholesterol are large, which is associated with a reduced risk of cardiovascular disease.

Your Apo ratio value is slightly elevated, which is because you have fairly high levels of LDL cholesterol and levels of HDL cholesterol that are in the lower range. A high Apo ratio increases the risk of cardiovascular diseases - but needs to be put in relation to other markers and health factors."

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#13

Ha, I think there are smarter people here than me!

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#14

I don’t think they differ in your case, it is too high even for the conservative/medicine 1.0 system. See the following link in Swedish where 5.0 mmol/L LDL speaks for familial hypercholesterolemia: Avancerade lipidrubbningar – utredning och behandlings­rekommendation - Janusinfo.se

You should def have Thomas Dayspring on :pray:

The most important thing is healthspan/lifespan IMO, not solely have to be about rapamycin.

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#15

I add you to the list of potential case report guests. I think you can provide good stuff!

#16

Sure. If you refer to any text book that covers basic hormone production you will see that all hormones come from a base of cholesterol. Advanced lipid testing is a better predictor, but more expensive and not as commonly used.

#17

I agree with this, but on your evidence based decision tree, this would be on the low side. No RCT to support this, but where expert opinion has a value!

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#18

Okay, I’ve already looked previously on this question and for example testosterone decreases by around -3% with statin usage. Just because hormones comes from cholesterol doesn’t mean it is a clinical significant effect.

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#19

Yes. My understanding is cells make their own cholesterol. The statins merely improve the liver’s ability to mop up the excess in the plasma. The body has an interesting reluctance to waste cholesterol. This must come from a time when the cost of making cholesterol and the scarcity of food made a difference. Not anymore.

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#20

I think you make good points and after reviewing the data on minimal change in testosterone levels with statin use see why you are skeptical.

In a world of extremes where the carnivore diet people are pushing messaging and the plant based diet (with better data) are pushing theirs, it can be confusing for the lay public and even medical professionals. I was hoping to give a suggestion that while it is important to get cholesterol low, that there may be levels that create consequences and considered too low. In clinical practice we don’t always have the advantage of RCT support everything we do. The expert opinions offered at many of the conferences I have attended for over 25 years suggest that there may be a too level of cholesterol and often point the basic hormone cascade as a reason we may want to be careful of going too low.

This site has a great combination of people with all back grounds, but the messaging can get muddy. If a LDL of 60 is great then 30 must be better, or if a Rapamycin dose of 6mg is good then 60mg must be better.

That being said, If I have a patient that has total cholesterol of 150, LDL of 60, normal advanced lipid testing and no plaque on a CIMT or calcium score that is on a statin drug, I would not increase their dose.

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#21

We already know the answer to the question that 30 LDL is better than 60 LDL…in clinical trials. So it is a false comparison.

#22

Dr. Thomas Dayspring pointed out this article on Twitter today. The full article is available. Once again supporting the evidence that very low LDL is not harmful;
“There’s compelling evidence that atherosclerosis occurs only when LDL particles enter the intimal space, which initiates the inflammatory cascade that is atherosclerosis. If there are no LDL particles in the intima, atherogenesis does not occur.2 This requires keeping circulating LDL-cholesterol (LDL-C) levels low enough (the lower, the better), decreasing them early enough (the earlier, the better), and maintaining them throughout one’s lifetime (the longer, the better), which early detection and modern treatments can readily achieve in nearly every case.”

“Many facts suggest that a desirable, physiologic level of LDL cholesterol is far lower than previously assumed”

“All cells of the body make their own cholesterol”

“Those born with complete absence of proprotein convertase subtilisin kexin type 9 (PSCK9; loss of function mutation) suffer no ill consequences from lifelong near zero circulating LDL-C and have no atherosclerosis.”

“There seem to be no significant adverse problems from LDL no matter how low it gets. Recent randomized studies and meta-analyses have also shown that even very low LDL-C (<25 mg/dL, < 0.67 mmol/L) does not increase risk for dementia or haemorrhagic stroke”.

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#24

there is a caveat. people who have low levels of cholesterol production can be at risk for cognitive decline if their cholesterol levels are suppressed. Dr Dayspring acknowledges that. it’s about 20-25% population and you can get cholesterol dynamics measured thru Boston Heart. i’m in that population so did quite a bit of research. Unfortunately lipid trials don’t stratify by sterol phenotype so hard to know if benefits are across board or mostly in the majority of the population that has average cholesterol synthesis levels

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#25

Yes, you are right. Especially lowering LDL-C with statins is questionable in APOE4 carriers (gene that predisposes you to dementia, I guess 25% of population carry it). I posted a video in topic about dementia. Before taking statins as primary prevention (especially with normal levels of cholesterol) one should consider at least APOE4 testing and possibly desmosterol levels test to decide whether statins are best option.

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#26

Thanks for sharing! In my population, it can be hard to get most people below 70 other than the truly motivated due to compliance of tolerating some of the higher doses of statins. Getting numbers as low as the 20s for LDL seems like a steep hill for the low risk population, but may be future.

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#27

Excellent podcast as always! I think this interview helped clarify for me where he is coming from. While he has become famous for his YouTube takes on various longevity topics, his philosophy on longevity is very much conservative and focusing on making sure everyone is taking care of those primary care basics of diet, exercise, sleep, blood pressure, cholesterol, stress… and his “extra credit” interventions are omega 3 and creatine.

And it’s a very sensible philosophy for a primary care doctor considering the vast majority of people are not even close to getting all the basics right, so basically even talking about the more exotic and less proven stuff that we talk about is not very sensible as a thing for him to focus on.

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#28

Wow, yea I’m on a statin and got my LDL down to 65 but… I don’t know what I would have to do to get it to 20. Definitely would have to throw some heavier drugs at it.

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#29

:pray: Yes, I agree that he is conservative but not as conservative as the most physicians as you point out. It will be very interesting to follow how his approach develops throughout the years and see if he gets more open or more conservative.

By the way, what statin are you using and how do you combine it with your rapamycin intake?

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#30

I’m on 10mg rosuvastatin. But also I’m currently taking a break from rapamycin… after I increased my dose from 2mg to 6mg, I started getting getting a ton of blood pressure related headaches and realized my bp was too high (140-150 systolic). I can’t be sure that the rapa was actually increasing the blood pressure or if it was coincidence, but I’m going to make sure my bp is stable for 6 months or so (taking losartan 100mg for that) before restarting my rapamycin, probably at a lower dose and tracking my bp.

It might not be connected, but this way I can isolate it as a factor as much as possible to see if there is an effect.

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